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Abramson Cancer CenterNCI CANCERLIT® Search: Adrenocortical Carcinoma - April 2002
National Cancer Institute®
Last Modified: April 1, 2002
Table of Contents
1
UI - 11484289
AU - Shon Ch; Mladenovski V; Petkov R; K'tev N; Mikhailov N; Gavrailov M;
TI -
Trifonov D
[Diagnosis and surgical treatment of adrenocortical carcinoma. A review
of the literature and report of two cases]
SO - Khirurgiia (Sofiia) 2000;56(2):45-9
Adrenocortical carcinomas (ACC) are rare and represent only 0.05 to 0.2%
of all cancers. They can be hormonally active, appearing clinically by
one or more endocrine syndromes, or can be hormonally non-active.
Commonly most of the cases with AC are diagnosed when the neoplastic
process have spread out of the suprarenal gland (stage III or IV).
Computed tomography and magnetic resonance imaging are the most useful
diagnostic methods of ACC but the latter is more accurate, especially in
estimation of the local invasion of the tumor. Surgery is the main and
the most effective method for treatment of both primary and recurrent
ACC, and in selective cases--of metastasis. The chemotherapy with
mitotane has a limited role and is indicated in cases of inoperable ACC
(primary or recurrent) and/or presence of metastasis. Two cases of ACC
treated in our department are reported. Case I: a 26-years-old female
with ACC in stage II, which was diagnosed incidentally by ultrasound
investigation for other consideration. Although the urine levels of free
cortisol were elevated, the woman had no endocrine symptoms. Case II: a
50-years-old female with a second recurrence ACC appeared 5 years after
a resection of the first recurrence tumor and 6 years after an operation
for the primary tumor. Problems in diagnose and surgical treatment of
these cases are discussed.
2
UI - 11889182
AU - Gao ZH; Suppola S; Liu J; Heikkila P; Janne J; Voutilainen R
TI -
Association of H19 promoter methylation with the expression of H19 and
IGF-II genes in adrenocortical tumors.
SO - J Clin Endocrinol Metab 2002 Mar;87(3):1170-6
AD - Department of Pathology, University of Helsinki, FIN-00014 Helsinki,
Finland.
Low H19 and abundant IGF-II expression may have a role in the
development of adrenocortical carcinomas. In the mouse, the H19 promoter
area has been found to be methylated when transcription of the H19 gene
is silent and unmethylated when it is active. We used PCR-based
methylation analysis and bisulfite genomic sequencing to study the
cytosine methylation status of the H19 promoter region in 16 normal
adrenals and 30 pathological adrenocortical samples. PCR-based analysis
showed higher methylation status at three HpaII-cutting CpG sites of the
H19 promoter in adrenocortical carcinomas and in a virilizing adenoma
than in their adjacent normal adrenal tissues. Bisulfite genomic
sequencing revealed a significantly higher mean degree of methylation at
each of 12 CpG sites of the H19 promoter in adrenocortical carcinomas
than in normal adrenals (P < 0.01 for all sites) or adrenocortical
adenomas (P < 0.01, except P < 0.05 for site 12 and P > 0.05 for site
11). The mean methylation degree of the 12 CpG sites was significantly
higher in the adrenocortical carcinomas (mean +/- SE, 76 +/- 7%) than in
normal adrenals (41 +/- 2%) or adrenocortical adenomas (45 +/- 3%; both
P < 0.005). RNA analysis indicated that the adrenocortical carcinomas
expressed less H19 but more IGF-II RNAs than normal adrenal tissues did.
The mean methylation degree of the 12 H19 promoter CpG sites correlated
negatively with H19 RNA levels (r = -0.550; P < 0.01), but positively
with IGF-II mRNA levels (r = 0.805; P < 0.001). In the adrenocortical
carcinoma cell line NCI-H295R, abundant IGF-II, but minimal H19, RNA
expression was detected by Northern blotting. Treatment with a cytosine
methylation inhibitor, 5-aza-2'-deoxycytidine, increased H19 RNA
expression, whereas it decreased IGF-II mRNA accumulation dose- and
time-dependently (both P < 0.005) and reduced cell proliferation to 10%
in 7 d. Our results suggest that altered DNA methylation of the H19
promoter is involved in the abnormal expression of both H19 and IGF-II
genes in human adrenocortical carcinomas.
3
UI - 11889190
AU - Lefebvre H; Cartier D; Duparc C; Lihrmann I; Contesse V; Delarue C;
TI -
Godin M; Fischmeister R; Vaudry H; Kuhn JM
Characterization of serotonin(4) receptors in adrenocortical
aldosterone-producing adenomas: in vivo and in vitro studies.
SO - J Clin Endocrinol Metab 2002 Mar;87(3):1211-6
AD - European Institute for Peptide Research (IFRMP 23), Department of
Endocrinology, INSERM, U-413, Centre Hospitalo-Universitaire de Rouen,
76031 Rouen, France. herve.lefebvre@chu-rouen.fr
We have previously shown that serotonin (5-HT) stimulates aldosterone
secretion from the human adrenal gland through activation of 5-HT(4)
receptors. The aim of the present study was to investigate in vivo and
in vitro the presence of 5-HT(4) receptors in aldosterone-producing
adenomas (aldosteronomas). Eight patients with aldosteronoma received a
single oral dose of placebo or cisapride (10 mg). Cisapride
administration significantly increased plasma aldosterone within 120 min
without any significant change in renin, cortisol, or potassium levels.
In two patients, a marked decrease in the plasma aldosterone response to
cisapride was observed after surgical removal of the tumor. The effects
of 5-HT and selective 5-HT(4) ligands on aldosterone production from
aldosteronoma tissues were studied in vitro using a perifusion system
technique. 5-HT and the 5-HT(4) receptor agonist cisapride (10(-7) M, 20
min) both stimulated aldosterone secretion from aldosteronoma slices.
The 5-HT- and cisapride-evoked aldosterone responses were inhibited by
concomitant administration of the specific 5-HT(4) receptor antagonist
GR 113808 (10(-7) M, 150 min). PCR amplification revealed the expression
of 5-HT(4) receptor mRNA in 13 of 14 aldosteronomas studied. Taken
together, these data show that most aldosteronomas, like normal
glomerulosa cells, express a functional 5-HT(4) receptor. Our results
also suggest that 5-HT, which can be locally released by intratumoral
mast cells, may play a role in the pathophysiology of these tumors.
4
UI - 11844057
AU - Honda K; Kashima K; Daa T; Gamachi A; Nakayama I; Yokoyama S
TI -
Myxoid adrenal cortical adenoma.
SO - Pathol Int 2001 Nov;51(11):887-91
AD - Department of Pathology, Oita Medical University, Oita, Japan.
hondak@oita-med.ac.jp
Myxoid adrenal cortical adenoma is a rare tumor and, to our knowledge,
only 16 cases have been reported. We present the case of a 56-year-old
Japanese man who was admitted to hospital because of a right adrenal
mass that was discovered during a routine physical examination. The
resected mass was well circumscribed and contained canary yellow
multinodular regions that were surrounded by a brown gelatinous region.
Histologically, the multinodular regions resembled a conventional
adrenal cortical adenoma, being composed of solid aggregates of large
clear or eosinophilic cells. In the gelatinous region, anastomosing
small eosinophilic or vesicular cells were visible within a myxoid
stroma that contained large amounts of acidic mucopolysaccharides.
Light-microscopic findings were consistent with a diagnosis of adenoma.
Immunohistochemical staining revealed that a small number of tumor cells
were positive for vimentin, and the MIB-1 labeling index was less than
1%. Flow cytometry demonstrated that cells were diploid. At the
ultrastructural level, many fat droplets were found in the large clear
cells in the multinodular regions. Small eosinophilic cells in the
myxoid region contained many mitochondria but few fat droplets. There
were no findings suggestive of malignancy. Although the adrenal cortex
might have the potential to produce connective tissue-type mucin as a
consequence of its mesodermal origin, the mechanism of production of
acidic mucopolysaccharides in a myxoid adrenal cortical tumor remains to
be clarified.
5
UI - 11921282
AU - Zhao J; Roth J; Bode-Lesniewska B; Pfaltz M; Heitz PU; Komminoth P
TI -
Combined comparative genomic hybridization and genomic microarray for
detection of gene amplifications in pulmonary artery intimal sarcomas
and adrenocortical tumors.
SO - Genes Chromosomes Cancer 2002 May;34(1):48-57
AD - Department of Pathology, University of Zurich, Zurich, Switzerland.
jianming.zhao@pty.usz.ch
Identification of gene amplifications in human tumors is important for
the understanding of tumorigenesis and may lead to discovery of
diagnostic and prognostic markers. In this study, we used a
microarray-based comparative genomic hybridization (CGH) technique,
combined with conventional CGH, to identify gene amplifications in 43
tumors including eight pulmonary artery intimal sarcomas and 35
adrenocortical tumors. Conventional CGH revealed gains or amplifications
of 12q13-q15 in six sarcomas and in two adrenocortical carcinomas. Using
microarrays, we demonstrated that, among genes located on 12q13-q15,
SAS/CDK4 were amplified in six sarcomas, and MDM2 and GLI in five and
four sarcomas, respectively. The two adrenocortical tumors showed
coamplifications of SAS/CDK4 and MDM2. Furthermore, PDGFRA (located on
4q12) amplification was identified in five sarcomas. Our data
demonstrate: (1) amplifications of SAS/CDK4, MDM2, GLI, and PDGFRA are
strongly associated with the tumorigenesis of pulmonary artery intimal
sarcomas, whereas SAS/CDK4 and MDM2 coamplification may contribute to
the progression of adrenocortical tumors; (2) microarray-based CGH is a
useful tool for simultaneous detection of multiple gene amplifications,
with a high sensitivity and resolution compared to that of conventional
CGH. Copyright 2002 Wiley-Liss, Inc.
6
UI - 11881068
AU - Felmeden DC; Gearty JG; Dawkins DM; Beevers G
TI -
Hypertension due to a giant aldosterone-secreting adenoma.
SO - J Renin Angiotensin Aldosterone Syst 2001 Mar;2(1):43-4
AD - Department of Medicine, City Hospital, Brimingham, UK.
felmeden@hotmail.com
7
UI - 11968809
AU - Naruoka T; Suzuki H; Ueda M; Kiyota H; Miki K; Ohishi Y
TI -
[A case of adrenocortical carcinoma with masculinization, obtaining long
prognosis with surgical treatment alone]
SO - Nippon Hinyokika Gakkai Zasshi 2002 Mar;93(3):499-503
AD - Department of Urology, Fuji General City Hospital.
A 28 year-old woman presented right upper abdominal pain. She had been
pointed out her masculinization and amenorrhea. CT scan and magnetic
resonance imaging showed right adrenal tumor. In the endocrinological
study, the serum cortisol and testosterone was elevated. Transabdominal
right adrenalectomy and nephrectomy was carried out and
histopathological diagnosis was adrenocortical carcinoma. The masculine
symptom had disappeared after the operation and she has been without
recurrence for five years.
8
UI - 11956997
AU - Hirano D; Okada Y; Ishida H; Takimoto Y; Okada K; Jike T
TI -
Morphometric analysis, at electron microscope level, combined with
hormone assay of nonfunctioning adrenocortical adenomas: comparison with
aldosterone-producing adenomas.
SO - Med Electron Microsc 2001 Dec;34(4):240-8
AD - Department of Urology, Nihon University School of Medicine, 30-1
Ooyaguchi Kamimachi, Itabashi-ku, Tokyo 173-8610, Japan.
byd04561@niftyserve.or.jp
We performed electron microscopic studies of eight nonfunctioning
adrenocortical adenomas (NFA) and nine aldosterone-producing adenomas
(APA) obtained from surgical specimens. A comparison of these two types
of adenomas was conducted by morphometric analysis of random electron
micrographs. The organelles measured included mitochondria (M),
smooth-surfaced endoplasmic reticulum (SER), rough-surfaced endoplasmic
reticulum (RER), lipid vacuoles (LV), and lysosomes (Ly). The content of
steroid hormones, including 17-alpha hydroxyprogesterone (17-OHP),
aldosterone (Ald), and other steroid hormones, was measured in adenoma
tissue from six NFA and eight APA. The percentages of the areas of the
organelles M, SER, and RER per total cell area in the NFA were
significantly lower than those in the APA. The average content of Ald in
adenoma tissues in APA was markedly higher than that in the NFA, while
the mean content of 17-OHP in the NFA was significantly higher than that
in APA. In conclusion, NFA are morphometrically characterized by a
reduction in organelles such as M, SER, and RER, compared with findings
in APA. From the quantitative analysis of steroid hormones, it was
suggested that NFA produce more precursor substances with less hormone
activity than APA and that steroidgenesis in NFA is shifted to a
glucocorticoid pathway, as indicated by the elevated 17-OHP
concentration.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
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